       Document 0380
 DOCN  M9640380
 TI    Trypsin inhibition: a potential cause of cobalamin deficiency common to
       the pathogenesis of Alzheimer-type dementia and AIDS dementia complex?
 DT    9604
 AU    McCaddon A; Regland B; Fear CF; Department of Clinical Neuroscience,
       Molndal Hospital of; Goteborg, Sweden.
 SO    Med Hypotheses. 1995 Aug;45(2):200-4. Unique Identifier : AIDSLINE
       MED/96104087
 AB    There is increasing evidence for an association between Alzheimer-type
       dementia (AD) and nutritionally independent cobalamin deficiency.
       Furthermore, low serum cobalamin values occur in a kindred with familial
       Alzheimer's disease (FAD) and histopathological confirmation of AD
       neuropathology. The Cobalamin deficiency could be either a consequence
       or cause of amyloidogenesis. Cobalamin deficiency is also associated
       with the acquired immunodeficiency syndrome (AIDS). A common pathogenic
       mechanism may exist for AIDS dementia complex (ADC) and AD, but there is
       no explanation at present for these associations. This paper presents
       the hypothesis that protease inhibition is a common factor in AD and ADC
       resulting in protein-bound cobalamin malabsorption and disrupted
       cobalamin metabolism.
 DE    Alzheimer's Disease/ETIOLOGY/*PHYSIOPATHOLOGY  AIDS Dementia
       Complex/ETIOLOGY/*PHYSIOPATHOLOGY  Human  Models, Biological
       Trypsin/*METABOLISM  *Trypsin Inhibitors  Vitamin B 12/METABOLISM
       Vitamin B 12 Deficiency/ETIOLOGY/*PHYSIOPATHOLOGY  JOURNAL ARTICLE
       REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

